G Protein-Coupled Receptors in the Control of Energy Homeostasis and Food Intake

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About this Research Topic

Submission deadlines

  1. Manuscript Submission Deadline 31 January 2025

  2. This Research Topic is still accepting articles.

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Background

The human genome encodes more than 900 different G protein-coupled receptors (GPCRs) yielding them the largest family of transmembrane proteins transducing extracellular signals into intracellular responses. GPCRs are seven transmembrane proteins that sense with high selectivity a diverse spectrum of signals including hormones, neurotransmitters, and many other signalling/bioactive molecules. They are expressed selectively on every cell type of the body underlying the relevance of these receptors in regulating a plethora of homeostatic responses. These features yield GPCRs major drug targets, indeed, GPCRs are the therapeutic target for a third of the pharmacological treatments currently available. However, an in-depth understanding of their roles as well as the involved signalling pathways is necessary to discover new potential pharmacological treatment options.


Agonist binding promotes conformational changes within the receptor and, thereby, activation of specific G proteins or G protein-independent processes such as the recruitment of β-arrestins. Recently, biased ligands that favor the recruitment of either G protein- or β-arrestin-mediated signalling pathways were identified, coining a new term called biased agonism, and opening a new world of possibilities. Thus, biased agonists can activate a therapeutic signalling pathway while avoiding the side effects associated with the other signalling pathway. A ground-breaking discovery in the field are the designer receptors exclusively activated by designer drugs or DREADDs, which are engineered human muscarinic receptors that respond exclusively to a synthetic compound such as clozapine-N-oxide (CNO). Additional modifications in the sequence have generated different versions of DREADDs that can selectively couple to distinct classes of G proteins or β-arrestin. Thus, when DREADDs are expressed in metabolically relevant cell types, in the presence of CNO, they modulate specific cell functions in a spatial and temporal resolution manner, hence, contributing to a better understanding of the physiological and pathological functions regulated by GPCRs. Another important milestone are transcriptomic data of single-cell RNA sequencing studies providing information about the selective expression of GPCRs in a subpopulation of cells in metabolic tissues. All these findings together have contributed to a better understanding of the functions regulated by GPCRs and their potential applications as therapeutic targets. However, the high potential of GPCRs is still being hampered by a large amount of so-called ‘orphan’ receptors with unknown ligands and/or signalling pathways.

Energy homeostasis and food intake are tightly regulated by different GPCRs expressed in central and peripheral cells. The neurobiological circuits that govern energy metabolism and feeding behaviour were evolutionary advantageous for the survival of the species. However, nowadays, the unprecedented access to highly and palatable food concomitant with our stressful and sedentary lifestyle overcomes thousands of years of evolution and are risk factors of the obesity epidemic and obesity-related disorders. The high prevalence of these metabolic disorders urges for new therapeutic interventions. Therefore, new insights of GPCR-related metabolic functions might shed light on the complexity of obesity and eating disorders to finally develop safer and more effective treatments.

This Research Topics welcomes submissions of (original research articles, brief research report, review, minireview, or commentary) focused, but not limited, to the following subtopics:

• GPCRs as regulators of homeostatic and hedonic food intake.

• GPCR-mediated regulation of rewarding and incentive properties of food (taste, odor, texture, appearance).

• GPCRs in energy homeostasis.

• GPCRs as targets of metabolic- and eating-related disorders.

• GPCR-mediated central and peripheral regulation of glucose and insulin homeostasis.

• GPCR-control of the microbiota-gut-brain axis.

• DREADD interventions of whole-body metabolism.

• Pharmacological approaches targeting GPCRs in the regulation of whole-body metabolism and metabolic and eating disorders.

• GPCR-related molecular signaling in peripheral and central tissue controlling whole body metabolism.

• Lipid regulation of GPCR signaling.

• Biased agonist of GPCRs in the control of energy homeostasis, food intake in physiological and pathological conditions.

• GPCR-mediated regulation of sympathetic activity and thermogenesis.

• Activation of GPCRs by ketone bodies in metabolic disorders.

Topic Editor Doreen Thor holds shares of Bayer AG . The other Topic Editors declare no competing interests with regard to the Research Topic subject.

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This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

  • Brief Research Report
  • Case Report
  • Clinical Trial
  • Data Report
  • Editorial
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

  • Brief Research Report
  • Case Report
  • Clinical Trial
  • Data Report
  • Editorial
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review
  • Opinion
  • Original Research
  • Perspective
  • Review
  • Study Protocol
  • Systematic Review
  • Technology and Code

Keywords: GPCR, G protein-coupled receptors, Energy homeostasis, food intake, rewarding, glucose, insulin, microbiota-gut-brain-axis

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